I wanted to introduce myself and share my background. I’m 23, and while I’ve been lurking on this forum for a few months, I actually started a heavy longevity supplement protocol when I was 20. That includes Rapamycin. I was initially pretty terrified of the side effects—specifically testicular atrophy and fatty liver seen in mouse models—but what finally sold me was Dr. Alan Green’s interviews and digging through the literature. It seems clear that intermittent dosing is the key to dodging those downsides.
I’m posting today because I need some help. I’ve noticed a lot of people here taking Bempedoic Acid and Ezetimibe. To be honest, I hadn’t heard of these being used in a longevity context before, so I’m really grateful for the insights this community provides.
I understand that the Bempedoic/Ezetimibe combo is great for lowering cholesterol and reducing the risk of a first cardiovascular event, but I’m worried about the trade-offs. I previously considered statins, but since they can promote vascular calcification, they seem like a better deal for middle-aged folks than for someone my age.
My question is: Can individuals with normal cholesterol levels preemptively take Bempedoic Acid and Ezetimibe for anti-aging purposes? Are there potential benefits to this approach, and what are the potential risks (similar to the risks associated with statins and aspirin mentioned above)?
Just to be clear, I have no intention of causing panic among people taking aspirin or statins. These risks apply specifically to younger populations and the evidence remains extremely limited. I am only using these examples to illustrate that the help I’m seeking is focused on these types of nuanced details.
Statins only promote vascular calcification if you already have plenty of soft plaque in your arteries. At it’s not promoting it per se as much as stabilizing the plaque. And plenty of studies even show regression of soft plaque to some degree.
They don’t have great evidence in young people because young people don’t usually die from heart attacks.
According to [Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms - PubMed], statins inhibit the synthesis of Vitamin K2, thereby reducing Matrix Gla Protein (MGP) levels. Simultaneously, they inhibit the biosynthesis of selenoproteins, which can accelerate vascular calcification. I am uncertain whether exogenous supplementation of Vitamin K2 and selenium can effectively counteract these specific side effects.
Furthermore, according to [Checking your browser - reCAPTCHA], even after adjusting for cholesterol levels and other risk factors, the annual progression rate of arterial calcification remains higher in statin users than in non-users.
Here we find a significant association between duration of statin therapy and total CACS. Specifically, long-term duration of statin therapy was significantly associated with a greater risk of having severe CACS. The increasing odds of having severe CACS being associated with higher duration of time on statin therapy remained significant after adjustment for the baseline cardiovascular risk factors known to significantly impact the CACS (ASCVD risk score, BMI, and CKD).
I’m not very familiar with the blockquote feature, so I apologize if the formatting is a bit messy.